Document Type
Article
Date of Original Version
2022
Department
Cell & Molecular Biology
Abstract
Dengue virus (DENV) infection is the most prevalent arthropod-borne virus disease and is endemic in more than 100 countries. Several DENV proteins have been shown to target crucial human host proteins to evade innate immune responses and establish a productive infection. Here we report that the DENV NS3 protein targets RIPK1 (Receptor Interacting Protein Kinase I), a central mediator of inflammation and cell death, and decreases intracellular RIPK1 levels during DENV infection. The interaction of NS3 with RIPK1 results in the inhibition of NF-κB activation in response to TNFR or TLR3 stimulation. Also, we observed that the effects of NS3 on RIPK1 were independent of NS3 protease activity. Our data demonstrate a novel mechanism by which DENV suppresses normal cellular functions to evade host innate immune responses
Publication Title, e.g., Journal
Frontiers in Cellular and Infection Microbiology
Volume
12
Citation/Publisher Attribution
Udawatte DJ, Lang DM, Currier JR, Medin CL and Rothman AL (2022) Dengue virus downregulates TNFR1- and TLR3-stimulated NF-kB activation by targeting RIPK1. Front. Cell. Infect. Microbiol. 12:926036. doi: 10.3389/fcimb.2022.926036
Available at: http://dx.doi.org/10.3389/fcimb.2022.926036
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.